title: Adipose and liver expression of interleukin (IL)-1 family members in morbid obesity and effects of weight loss.
abstract: Morbid obesity is associated with a state of chronic inflammation. Interleukin-1 family (IL-1F) cytokine members are produced by human adipose tissue in obesity. Whereas certain IL-1F members such as IL-1β or IL-18 are potently proinflammatory, others such as IL-1 receptor antagonist (IL-1Ra) or IL-37 (formerly IL-1F7) are antiinflammatory. The NLRP3 inflammasome plays a key role in the processing of bioactive IL-1β and IL-18. We investigated the effect of excessive weight loss on subcutaneous adipose tissue and liver expression of IL-1α, IL-1β, IL-18, IL-1Ra, IL-37 and NLRP3. Twenty-one severely obese patients undergoing laparoscopic adjustable gastric banding were studied. Tissue samples were collected before and 6 months after laparoscopic adjustable gastric banding surgery. mRNA expression of all studied IL-1F members, but especially of IL-37, was much higher in subcutaneous/visceral adipose tissue compared with their liver expression. Subcutaneous adipose tissue mRNA expression of IL-1β decreased significantly after extensive weight loss; expression of IL-18 and IL-1Ra did not change, whereas IL-37 expression increased. Weight loss led to a significant reduction in liver IL-1β, IL-18 and IL-1Ra expression, whereas hepatic IL-37 mRNA expression remained stable. Adipose/liver NLRP3 inflammasome and IL-1α expression were not affected by weight loss. Tissue expression of IL-1β, IL-18 and IL-37 were significantly higher in subcutaneous/visceral adipose tissue compared with the liver. In conclusion, expression of IL-1F members is more pronounced in adipose compared with liver tissue in patients with severe obesity. Excessive weight loss changes the adipose and liver expression profile of IL-1F members toward a more antiinflammatory direction.
authors.affiliation: Christian Doppler Research Laboratory for Gut Inflammation, Medical University Innsbruck, Innsbruck, Austria.
authors.forename: Alexander R
authors.initials: AR
authors.lastname: Moschen
authors.forename: Clemens
authors.initials: C
authors.lastname: Molnar
authors.forename: Barbara
authors.initials: B
authors.lastname: Enrich
authors.forename: Sabine
authors.initials: S
authors.lastname: Geiger
authors.forename: Christoph F
authors.initials: CF
authors.lastname: Ebenbichler
authors.forename: Herbert
authors.initials: H
authors.lastname: Tilg
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000368:Aged; D002352:Carrier Proteins / Q000235:genetics; D005260:Female; D015391:Gastroplasty / Q000379:methods; D020869:Gene Expression Profiling; D006801:Humans; D058847:Inflammasomes / Q000235:genetics; D053590:Interleukin 1 Receptor Antagonist Protein / Q000235:genetics; D007375:Interleukin-1 / Q000235:genetics*; D020382:Interleukin-18 / Q000235:genetics; D053582:Interleukin-1alpha / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics; D008099:Liver / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D009767:Obesity, Morbid / Q000235:genetics* / Q000601:surgery; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D015431:Weight Loss; D055815:Young Adult
chemical_list: D002352:Carrier Proteins; C508587:IL37 protein, human; D058847:Inflammasomes; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D020382:Interleukin-18; D053582:Interleukin-1alpha; D053583:Interleukin-1beta; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C453881:NLRP3 protein, human